We have produced blood typing reagents which define blood groups in rhesus monkeys. Using them as genetic markers, we found that monkey mothers can be immunized against incompatible blood factors carried by fetal red cells which cross the placenta. These antibodies pass from mother to fetus and actually coat the cells of the newborn. However unlike humans nothing seems to happen no matter which of the blood factors is involved. We intentionally immunized females throughout their pregnancies with blood from their mates and even these very potent antibodies did not destroy the newborn's cells. Also, we were unable to cause hemolytic disease by injecting potent antibody directly into the newborn monkey. To find out what protects the newborn from hemolytic disease we injected radioactive-labelled blood cells coated with antibody and measured their rate of removal from the circulation. They were removed at the same rate or perhaps even slower than red cells that were not coated with antibodies. We are now trying to find out if there is a missing receptor on the macrophages that normally remove antibody-coated cells from the circulation. The answer to the question of why rhesus babies don't get hemolytic disease is likely to help us understand hemolytic disease in human babies.